• =?UTF-8?Q?Alpha=2DLinolenic_Acid_Against_Alzheimer=E2=80=99s?=

    From ironjustice@21:1/5 to All on Tue May 8 10:26:08 2018
    Neuroprotective Effect of Alpha-Linolenic Acid against Aβ-Mediated Inflammatory Responses in C6 Glial Cell
    Ah Young Lee† , Myoung Hee Lee‡, Sanghyun Lee*§, and Eun Ju Cho*†
    † Department of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Republic of Korea
    ‡ Department of Southern Area Crop Science, National Institute of Crop Science, Rural Development Administration, Gyeongnam 50424, Republic of Korea
    § Department of Integrative Plant Science, Chung-Ang University, Gyeonggi 17546, Republic of Korea
    J. Agric. Food Chem., Article ASAP
    DOI: 10.1021/acs.jafc.8b00836
    Publication Date (Web): April 18, 2018
    Copyright © 2018 American Chemical Society
    *E-mail: (S.L.) slee @ cau.ac.kr. Phone: 82-31-670-4688., *E-mail: (E.J.C.) ejcho @ pusan.ac.kr. Phone: +82-51-510-2837. Fax: +82-51-583-3648.
    Cite this:J. Agric. Food Chem.

    Abstract Image
    Therapeutic approaches for neurodegeneration, such as Alzheimer’s disease (AD), have been widely studied. One of the critical hallmarks of AD is accumulation of amyloid beta (Aβ). Aβ induces neurotoxicity and releases inflammatory mediators or
    cytokines through activation of glial cell, and these pathological features are observed in AD patient’s brain. The purpose of this study is to investigate the protective effect of alpha-linolenic acid (ALA) on Aβ25–35-induced neurotoxicity in C6
    glial cells. Exposure of C6 glial cells to 50 μM Aβ25–35 caused cell death, overproduction of nitric oxide (NO), and pro-inflammatory cytokines release [interleukin (IL)-6 and tumor necrosis factor-α], while treatment of ALA increased cell viability
    and markedly attenuated Aβ25–35-induced excessive production of NO and those inflammatory cytokines. Inhibitory effect of ALA on generation of NO and cytokines was mediated by down-regulation of inducible nitric oxide synthase and cyclooxygenase-2
    protein and mRNA expressions. In addition, ALA treatment inhibited reactive oxygen species generation induced by Aβ25–35 through the enhancement of the nuclear factor-erythroid 2-related factor-2 (Nrf-2) protein levels and subsequent induction of heme-
    oxygenase-1 (HO-1) expression in C6 glial cells dose- and time-dependently. Furthermore, the levels of neprilysin and insulin-degrading enzyme protein expressions, which contribute to degradation of Aβ, were also increased by treatment of ALA compared
    to Aβ25–35-treated control group. In conclusion, effects of ALA on Aβ degradation were shown to be mediated through inhibition of inflammatory responses and activation of antioxidative system, Nrf-2/HO-1 signaling pathway, in C6 glial cells. Our
    findings suggest that ALA might have the potential for therapeutics of AD.

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